My work centers on the mechanism of action of hormones which alter fluid and electrolyte transport - the primary focus being the action of aldosterone. The physiological effects of aldosterone require a receptor-mediated rise in RNA and protein synthesis. The induced proteins are thought to work at several key sites in the cell, - sites which govern rate-limiting processes for the transport of Na, K and H ions. In general, all of the suggested pathways by which aldosterone-induced proteins act, are thought to ultimately affect either the entry of Na into the cell, the provision of energy or substrate for transport, or the coupling ratio/level of functional Na-K ATPase molecules. However, most of the above thesis is predicated on studies on toad bladder. In the past, my work has involved several facits of this model including characterization of both the cytoplasmic mineralocorticoid receptor and the chromatin-binding site for receptor complexes. Because continuation of these studies was hampered by lack of defined target site(s) along the mammalian nephron, we exploited the use of citrate synthase (CS), a biochemical marker of aldosterone-sensitive sites, to help identify cellular targets for aldosterone in the rabbit kidney. Those sites which showed maximal aldosterone-sensitive changes in CS activity were the cortical collecting tubule (CCT) and the medullary thick ascending limb of Henle (mTALH). In parallel studies, we also determined that aldosterone increased Na-K ATPase activity in the CCT. The current research plan furthers our developing model of aldosterone action in the mammalian kidney by examining the role of intracellular Na in the activation of both CS and Na-K ATPase activities in the CCT, as well as the physiological role of aldosterone in the mTALH.